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Neuro 210 > Pain: A neurobiological perspective > Flashcards

Pain: A neurobiological perspective Flashcards

1
Q

How does the international association for the study of pain (IASP) describe what pain is?

A

an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage

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2
Q

What are 2 types of pain? describe.

A
  1. nociceptive pain (day to day pain); it is stimulated by a noxious stimuli like heat, cold, mechanical force or chemical irritants; results in adaptive, high-threshold pain and it is protective and early warning
  2. Pathological pain (non-adaptive pain); stimulated by neuropathic pain like neural lesion or positive and negative symptoms; which is usually a result of some type of damage of neurons in PNS and CNS which leads to maladaptive, low threshold pain
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3
Q

What are the spinal cord levels?

A
  1. Cervical C1-C5
  2. Thorasic T1-T12
  3. Lumbar L1-L5
  4. Sacral S1 - S2

each division corresponds to a level in the spinal cord

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4
Q

Where do Primary sensory neurons live? (PSN)

A

in the dorsal root ganglions

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5
Q

What are the types of primary sensory neurons? and their properties

A
  1. large light PSN aka A-alpha and A-beta fibers
    which are to discriminate touch and proprioception (not typical pain cells)
  2. Small dark PSN aka A-delta and C fibers which respond to pain and temperature
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6
Q

what are the properties of A-alpha and A-beta fibers?

A
  • they are myelinated and large and they conduct impulses rapidly towards proprioception and light touch
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7
Q

What are the properties of A-delta fibers?

A
  • they are lightly myelinated
  • medium diameter
  • and involved in nociception of mechanical, thermal and chemical stimuli
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8
Q

What are the properties of c-fibers

A

unmyelinated

  • small diameter
  • responds to noxious temp and itch as well as nociception

conducts super slowly and known as “secondary pain” because u feel it after the first pain response

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9
Q

What is the specificity theory of pain?

A

suggests that we have a system dedicated for transmitting noxious stimuli

  • suggested by decartes in 1664 and theres a direct, invariant relationship between a psychological sensory dimension and a physical stimulus
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10
Q

What does the gate theory of pain suggest?

A

that pain can be modulated

  • there is a “gate” within the spinal cord that gets opened or closed
  • in reality, gate cells are inhibitory neurons and interneurons that will either allow or close off impulses getting into the spinal cord from the sensory systems and distrupts it getting to the brain to be processed further
  • A delta and and c- fibers shut off gate cells and open the gate, the large A-beta fibers activate the gate cell and close it to dampen the pain
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11
Q

What is significant about the pain pathways-sensitization?

A

pain processing is very dynamic and plastic

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12
Q

What is hyperalegsia?

A

its when signals of pain are amplified (response is amplified)

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13
Q

what is allodynia?

A

paradoxial pain, where pain towards something that isnt supposed to be painful (pain towards previously innocuous stimuli)

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14
Q

What function does the dynamic-ness of pain pathways serve?

A

it can be protective for us

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15
Q

What levels can sensitization (amplification towards pain) occur?

A

at peripheral level and at central level

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16
Q

How does peripheral sensitization occur?

A

There are mediators of pain upon first contact in the “inflammatory soup” formation, like 5-HT, bradykinin, histamine..etc..
- these mediators dont directly activate a nocicpetor, they bind to receptors ON nociceptors and trigger a second messenger cascade that sensitizes and changes properties of nerve endings therefore, any stimulus that follows will either be amplified or dampened

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17
Q

What is the step by step process of peripheral sensitization?

A

a mediator like prostaglandin binds to a receptor on the nociceptor (like a-alpha or b-alpha) and that releases a g-protein to go out and activate an enzyme like PKA. PKA activated by G-protein, then phosphorylates sodium channels and changes its conformations, and therefore changes how much sodium enters and the response to the next stimulus

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18
Q

What happens if you reduce threshold for activation in peripheral sensitization?

A

there will be more firing of the neuron responsible for pain signalling

19
Q

what happens if you increased the output to a given stimulus and then put in in prostaglandin solution?

A

it fires rapidly (high frequency) and low amplitude

20
Q

What is plasticity in the pain pathways in central sensitization under normal conditions?

A

in normal excitatory amino acid released, we have normal activation of AMPA receptors and NMDA receptors are silent because of the mg2+ blockage

21
Q

What is plasticity in the pain pathways in central sensitization under sensitized conditions?

A

enhanced EAA released of neuropeptides
- NMDA receptors open up because of the depolarization
calcium enters the cell and causes acute phosphorylation and also causes long term gene transcription
- a reduced threshold will increase the input

22
Q

what is a windup occurrence in CNS?

A

it is homosynaptic activity dependant plasticity. basically stimulating the spinal cord with painful stimulus at a certain frequency and looking at the activity of cfibers
- the summations of potentials recruits NMDA’rs

23
Q

What is heterosynaptic activity dependent activity in CNS?

A

its when u present a small, below threshold touch to someone and then bommbarard it with intense c-fiber targetting stimulus and then presentikng the low stimulus agaiin and seeing how much the cell fires to the low one bc its sensitized

24
Q

what are the properties of chronic pain?

A

pain that presists beyond the time it takes to heal

  • it is maladaptive
  • wrong processing activity in the system may establish some type of sensitization but other factors like gene transcription and structural organization account for the persistence of chronic pain
  • glial cells in CNS like astrocytes and microglia are now recognised s critical mediators of this process
25
Q

WHat are glial cells?

A

they consist of astrocytes and microglia

  • they are mediators of hemostasis that “listen” and “talk” to neurons for their needs
  • highly responsive to perturbations and become “reactive”
  • they are sensitive to large changes in extracellular environment
26
Q

how do reactive glial cells mediate sensitization?

A

pain stimuli sends glial cells into a reactive state and in this state, astrocytes and microglia secret factors that can act back to the neurons (glial cells become part of the synapse) and they enhance PTN excitability (LTP/NMDA) and enhance primary afferent substances P and EAA release

27
Q

What is one way to reverse neuropathic pain?

A

to inhibit glial reactivity

  • metabilic inhibitors can prevent the proliferation and activation of astrocytes and microglia
  • effecively prevent/reverse neuropathic pain behaviors in rodent moels with a drug called PPF (it just reduces the number of microglia that react to a change in the NS)
28
Q

what are 2 other names of glial modulating agents that show similar efficacy

A
  1. fluorcitrate

2. minocycline

29
Q

What are the two major pathways from the spinal cord to the brain? Where do these tracts pass through?

A

the spinothalamic tract and the spinoreticular tract

projections to the reticular formation, thalamus (VPL, intralaminar) and somatosensory cortex areas

from brain to spinal cord it passes through PAG to RVM to dorsal horn

30
Q

Which areas in the brain can pain be either amplified or dampened to spinal cord?

A

at PAG or RVM

31
Q

What are the 3 dimensions of pain?

A
  1. sensory-discriminative –> location, intensity and duration
  2. affective-motivational –> unpleasantness and quality
  3. cognitive evaluative –> attention, anticipation and memory (has similarities between memory and learning)
32
Q

Which areas of the brain is associated with sensitivity to pain and pain response?

A

pain elicits distinct patterns of activation in cortical and subcortical regions
- SI and SII, thalamus, ACC and anterior insula play a role in pain activation
the ACC is the anterior cingulate cortex and its activity is related to attention
- the insula links with the limbic system structures and suggests role in affective/ reactive emotional responses to pain

33
Q

What condition to people with insular lesions report?

A

pain asymbolia –> inappropriate emotional reaction to pain

34
Q

What is the relationship between intensity coding regions in the brain in response to pain and attentional networks in the brain? How does this show that the brain is dynamic?

A

if we focus our attention on the painful stimulus then we get more activation of the intensity coding regions (more intensity of pain comes through)

  • if we dont focus on the pain but dont focus on anything else either, then we get moderate or neural pain activation
  • if we do something else/distract ourselves while feeling painful stimulus then we get a diverisve response and we feel less pain going through

in all cases the stimulus is the same but the pain is processed differently in the brain based on attention levels

35
Q

How has empathy been shown to play a role in pain processing?

A

the same areas responsible to fire when we are in pain fire when we view others in pain (minus the somatosensory and motor areas)

  • areas like the ACC, the thalamus, and the anterior insular all become active when we view others in pain and when we are in pain
36
Q

What is congenital insensitivity to pain?

A

its a rare clinical syndrome that is characterized by dramatic impairements in the ability to detect pain from pain and onwards and its caused by heriditary neuropathy or channelopaty

either their nociceptors dont develop properly, or they have HSAN IV (a mutation for trkA) which causes nociceptors like c-fiber cells to not develop, or channelopahty associated with insensitivity to pain through wrong structure conformation of the sodium channels Nav 1.7

37
Q

How do the brains of patients with CIP respond when viewing pain in others?

A

their pain regions light up as if they were experiencing pain themselves

38
Q

What are three ways you can peripherally treat pain?

A

1) simpliest way is to use NSAIDs like ibuprofen to block Prostaglandin and other mediators
2) using opiods to activate the inhibitory g-proteins which slows down the PKA production (second messenger production) and leads to closing of the sodium channels
3) acting on the sodium channel directly using a local anesthetic like lidocaine to shut everything off and prevent AP

39
Q

How to centrally treat pain?

A

When dealing with non-neuropathic pain (pain not associated with damaged nerves) then drugs that target opioid receptors and ca2+ channels prevent transmitter release and decrease output of second order neurons
- opiods dont work on neuropathic pain and chronic use because it increases the microglia present in the cell after tolerance and causing hypersensitivity when withdrawn from

40
Q

How do anti depressants treat pain?

A

antidepressants elevate 5-ht levels and that can inhibit spinal neurons

  • it elevates levels of inhibitory transmitters like serotonin in CNS which dampens excitations in cells
  • includes drugs like SNRI’s and TCA’s
41
Q

how to SNRI’s treat neuropathic pain?

A

Serotonin-norepinephrine reuptake inhibitors elevate levels of 5HT and NE in the synaptic cleft which are both inhibitory and dampens excitations
- a drug called duloxetine is approved for neuropathic pain and fibromyalgia

42
Q

What are some examples of drugs (2) that are calcium channel blockers?

A
  • block ca2+ channels and dampen pain

- 2 antidepressants in TCA field called gabapentin or pregabalin (gaba)

43
Q

What is an example of a sodium channel blocker drug?

A

SNRI antidepressants called topical lidocaine

44
Q

What is an opiod used to reduce pain?

A

tramadol or CR opiod analgesic

Neuro 210 (12 decks)

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